Alterations in acid-base balance and high-intensity exercise performance after short-term and long-term exposure to acute normobaric hypoxic conditions

Abstract

This investigation assessed the course of renal compensation of hypoxia-induced respiratory alkalosis by elimination of bicarbonate ions and impairments in anaerobic exercise after different durations of hypoxic exposure. Study A: 16 participants underwent a resting 12-h exposure to normobaric hypoxia (3,000 m). Blood gas analysis was assessed hourly. While blood pH was significantly increased, PO₂, PCO₂, and SaO₂ were decreased within the first hour of hypoxia, and changes remained consistent. A substantial reduction in [HCO₃^-] levels was observed after 12 h of hypoxic exposure (- 1.35 ± 0.29 mmol/L, p ≤ 0.05). Study B: 24 participants performed in a randomized, cross-over trial portable tethered sprint running (PTSR) tests under normoxia and after either 1 h (n = 12) or 12 h (n = 12) of normobaric hypoxia (3,000 m). No differences occurred for PTSR-related performance parameters, but the reduction in blood lactate levels was greater after 12 h compared with 1 h (- 1.9 ± 2.2 vs 0.0 ± 2.3 mmol/L, p ≤ 0.05). These results indicate uncompensated respiratory alkalosis after 12 h of hypoxia and similar impairment of high-intensity exercise after 1 and 12 h of hypoxic exposure, despite a greater reduction in blood lactate responses after 12 h compared with 1 h of hypoxic exposure.

Figure 1

Study A: time course for (a) blood bicarbonate concentration ([HCO₃⁻]) and active base excess (BE), (b) oxygen partial pressure (PO₂) and carbon dioxide partial pressure (PCO₂), and (c) arterial oxygen saturation (SaO₂) and blood pH (pH_b) under normoxic conditions (PRE) and during 12 h of exposure to a simulated altitude of 3,000 m (HYP1–HYP12) in participants of Study A (n = 16). Data points represent mean ± standard deviation for [HCO₃⁻], PO₂, and SaO₂ (filled triangle), and BE, PCO₂, and pH_b (filled riangle). See “Methods” section for further details. *p ≤ 0.05 compared with PRE.

Figure 2

Study A: reduction in blood bicarbonate concentration ([HCO₃⁻]) after 12 h of exposure to a simulated altitude of 3,000 m (Δ [HCO₃⁻] = [HCO₃⁻] HYP12 − [HCO₃⁻] PRE) in male (n = 9) and female (n = 7) participants. Data points represent individual values (open circle) and mean ± SD (filled circle) for Δ [HCO₃⁻]. An “x” indicates female participants with oral contraceptive ingestion. See “Methods” section for further details. *p ≤ 0.05 compared with the corresponding values in male participants.

Figure 3

Study B: performance measurements in the 1-h hypoxia group (G1) (n = 12) and the 12-h hypoxia group (G12) (n = 12) under normoxia (NOR) and after 1 or 12 h of hypoxic exposure (HYP), respectively, for (a) peak force (PF), (b) mean force (MF), (c) the fatigue index (FI), and the associated physiological response of (d) maximum post-exercise lactate concentration (La_max). ∆ values (HYP − NOR) indicate intra-individual hypoxic-induced changes in performance parameters. Data points represent individual values (open circle). Bar charts show mean ± standard deviation. *p ≤ 0.05 compared with NOR. See “Methods” section for further details.